Structure of a myelinated motor neurone

A motor neurone is a nerve cell that carries impulses from the central nervous system towards an effector, such as a muscle or gland. Its parts are arranged along the path taken by the impulse.

The cell body contains the nucleus. Branched dendrites extend from the cell body and receive signals from other cells. A long axon carries impulses away from the cell body. At its far end, the axon divides into branched axon terminals, which connect with the effector.

Myelin sheath and nodes of Ranvier

In a myelinated motor neurone, sections of myelin sheath surround the axon. In the peripheral nervous system, these sections are formed by Schwann cells. The myelin electrically insulates the axon membrane.

There are gaps between successive sections of myelin, called nodes of Ranvier. At each node, a small region of the axon membrane is exposed. The gaps are in the sheath, not breaks in the axon.

Resting potential

A neurone that is not transmitting an action potential has a difference in electrical potential across its membrane: the inside is negative relative to the outside. This difference is the resting potential. It depends on unequal concentrations of ions on the two sides of the membrane and on how readily those ions can cross it.

Maintaining the ion concentrations

The sodium–potassium pump uses energy from ATP to move three sodium ions ($$\ce{Na+}$$) out of the neurone for every two potassium ions ($$\ce{K+}$$) it moves in. It maintains a higher sodium ion concentration outside the neurone and a higher potassium ion concentration inside.

Potassium movement and the resting potential

At rest, the membrane is more permeable to potassium ions than to sodium ions. Potassium ions therefore diffuse out through leak channels, down their concentration gradient. As positive ions leave, the inside becomes negative relative to the outside.

The negative interior attracts potassium ions back towards the inside. This electrical attraction opposes their outward diffusion: the concentration gradient favours movement out, while the electrical difference favours movement in.

Some sodium ions also leak into the neurone. The resting potential reflects the balance between the concentration and electrical influences on ion movement, together with this small sodium leak and the continued action of the sodium–potassium pump.

Action potential generation

An action potential is a rapid, temporary change in the electrical potential across a neurone’s membrane. At rest, the inside of the neurone is negative relative to the outside. During an action potential, the inside briefly becomes positive before returning towards its resting value.

Depolarisation and sodium entry

A stimulus can make the membrane potential less negative. This change is called depolarisation. If depolarisation reaches a level called the threshold, voltage-gated sodium channels open. These channels increase the membrane’s permeability to sodium ions, $$\ce{Na+}$$.

Sodium ions enter the neurone down their electrochemical gradient. Their entry makes the inside more positive, causing further depolarisation. This opens more voltage-gated sodium channels, allowing more sodium ions to enter. As a result, the membrane potential rises rapidly and becomes positive inside relative to outside.

Repolarisation and hyperpolarisation

The sodium channels then inactivate, stopping sodium entry through them, and voltage-gated potassium channels open. Potassium ions, $$\ce{K+}$$, leave the neurone, making the inside negative again. This return towards a negative membrane potential is called repolarisation.

Potassium channels do not close immediately, so potassium ions continue to leave for a short time. The membrane potential briefly becomes more negative than its resting value; this is hyperpolarisation. The potassium channels then close and the resting potential is restored.

The all-or-nothing principle

An action potential occurs only if depolarisation reaches threshold. A stimulus that does not bring the membrane to threshold does not produce an action potential. Once an action potential is triggered, a stronger stimulus does not make it larger.

Action potential propagation

A nerve impulse travels along an axon because an action potential at one region of the membrane triggers a new action potential in the next region. The original action potential does not simply travel unchanged along the axon: it is regenerated at successive positions.

Local currents and regeneration

During an action potential, sodium ions enter the axon, making the inside of that region less negative. This depolarisation creates local currents: positive charge spreads within the axon towards an adjacent region of membrane.

The local currents depolarise the adjacent membrane. If it reaches threshold, voltage-gated sodium channels open there. Sodium ions enter, generating a new action potential. This action potential then creates local currents that depolarise the next region. The impulse can therefore continue along the axon rather than simply fading as the local current spreads.

Propagation in non-myelinated and myelinated axons

In a non-myelinated axon, local currents trigger action potentials in successive regions of membrane along the axon. Each newly depolarised region triggers the region next to it.

In a myelinated axon, myelin insulates the membrane between gaps called nodes of Ranvier. Local currents spread beneath the myelin and depolarise the membrane at the next node to threshold. A new action potential is generated there, and the process continues at successive nodes.

This is called saltatory conduction: the impulse effectively travels from node to node, with action potentials regenerated at the nodes rather than along every region of membrane between them.

Refractory period

After an action potential, a section of nerve cell membrane cannot immediately produce another one as easily. This interval is called the refractory period. At first, another action potential cannot be generated; later, it can be generated, but only by a stronger-than-usual stimulus.

Changes in membrane excitability

Immediately after an action potential, voltage-gated sodium channels are inactivated and cannot reopen immediately. During this absolute refractory period, another action potential cannot be generated, regardless of the strength of the stimulus.

As the sodium channels recover, another action potential becomes possible. However, potassium permeability may remain high, allowing potassium ions to continue leaving the cell. This can make the inside of the membrane more negative than at rest, a state called hyperpolarisation. During this relative refractory period, a stronger-than-usual stimulus is needed to bring the membrane to the level required to generate an action potential. Excitability returns towards normal as the membrane returns towards its resting state.

Effects on nerve impulses

The refractory period separates successive action potentials into discrete impulses and limits how frequently they can be generated.

It also helps an impulse travel forwards along a nerve cell. As an action potential advances, the membrane just behind it is temporarily unable to generate another action potential, so the impulse does not normally reactivate that region and travel backwards.

Factors affecting nerve impulse conduction speed

A nerve impulse travels along an axon as changes in the membrane’s electrical state trigger new action potentials farther along it. Local currents spread from an active region to the next region, bringing its membrane to the threshold needed to trigger an action potential. Myelination, axon diameter and temperature affect how quickly this happens.

Myelination and conduction speed

Myelin insulates the axon membrane between gaps called nodes of Ranvier. Local currents spread beneath the myelin to the next node, where they bring the membrane to threshold and regenerate the action potential. The impulse therefore appears to jump from node to node rather than generating an action potential along every part of the membrane. This is called saltatory conduction and increases conduction speed.

Axon diameter and conduction speed

A larger axon diameter reduces resistance to the flow of local currents inside the axon. The currents can therefore spread more readily, bringing the next region of membrane to threshold more quickly. As a result, impulses generally travel faster along larger-diameter axons.

Temperature and conduction speed

Within a suitable physiological range, a higher temperature increases the rates of ion movement and the processes by which ion channels operate. This generally increases conduction speed. Cooling slows these processes, so the impulse travels more slowly.